BY

dr. WIDODO S., MKes

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HORMONE  ORGANIC SUBSTANCE PRODUCED BY ENDOCRINE GLAND

SITE OF ACTIVITY HORMONE :

TARGET CELL or TARGET ORGAN

1. AUTOCRINE TISSUE
 . H. TESTOSTERON; H. OESTROGEN
2. PARACRINE TISSUE

NEEDS RECEPTOR / MEDIATOR

RECEPTORE :
• HORMONE BIND RECEPTOR OF TARGET CELL
• RECEPTORE ARE PROTEIN
• RECEPTORE CAN CONFLUENCE ACTIVITY OF HORMONE
• HORMONES HAS ONE OR MANY RECEPTORES

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CLASSIFICATION OF HORMONES BY MECHANISM OF ACTION :

1. HORMONES THAT BIND TO INTRACELLULAR RECEPTOR S :

STEROID HORMONE, THYROID HORMONE. CALCITRIOL
2. HORMONES THAT BIND TO SURFACE RECEPTORS :
II.1. THE SECOND MESSENGER IS c AMP
-. H. ADENOHIPOFISE -. H. HIPOFISE POSTERIOR
-. MSH; etc

II.2. THE SECOND MESSENGER ARE Ca++ / FOSFATIDIL INOSITOL

: ASETIL KOLIN, GASTRIN, VASOPRESIN, ADH
OKSITOSIN.
II.3. SECOND MESSNGER IS KINASE atau PHOSPHATE :
GROWTH HORMONE, PROLAKTIN, INSULIN

MEDIATOR IS CALLED SECOND MESSENGER

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HORMONE IS CALLED FIRST MESSENGER
MEKANISME KERJA HORMON :

KELOMPOK I : HORMON DALAM SEL IKATAN

DENGAN RESEPTOR KOMPLEKS H-R
AKTIVASI IKATAN DENGAN GENE
atau DNA HRE SINTESA PROTEIN
atau TRANSKRIPSI
KELOMPOK II : HORMON MENEMPEL & BERIKATAN
DENGAN RESEPTOR MEDIATOR :
cAMP, Fosfatidil Inositol, Ca++
FUNGSI FISIOLOGIS JARINGAN SASARAN

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GROUP I HORMONE : ALTER GENE EXPRESSION
GROUP II HORMONE

- BINDS MEMBRANE RECEPTOR

- USE INTRACELLULAR MESSENGERS

EXAMPLE OF INTRACELLULAR MESSENGER :

- cyclic AMP
- cyclic GMP
- CALCIUM
- PHOSPHATIDYLINOSITOLS
HORMONE ACTION WITH CYCLIC AMP AS INTRACELLULAR MESSENGERS
HORMONE ACTION WITH CYCLIC GMP AS INTRACELLULAR MESSENGERS
HORMONE ACTION WITH CACIUM AS INTRACELLULAR MESSENGERS

CALCIUM CONCENTRATION :

EXTRACELL : 5 MMOL/L
INTRACELL : 0.1 – 10 MICROMOL/L

10,000 FOLD DIFFERENCE

CALMODULIN
 PITUITARY GLAND
( HORMON HIPOFISE )

1. LOBUS / PARS ANTERIOR = ADENOHIPOFISE :

- GH - FSH - LH
- TSH - ACTH - LTH
2. LOBUS / PARS INTERMEDIA : MSH

3. LOBUS / PARS POSTERIOR = NEUROHIPOFISE :

- OKSITOSIN
- VASOPRESIN = ADH
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HYPOTHALAMUS AND PITUITARY GLAND
HYPOTHALAMIC HORMONE
HYPOTHALAMIC AND PITUITARY HORMONE INTEGRATION
GROWTH HORMONE (GH), PROLACTIN (PRL)

AND

CHORIONIC SOMATOMAMOTROPIN (CS)

 GROWTH HORMONE = GH

► STRUCTURE : POLIPEPTIDE

► SYNTHESIS :
SYNTHESZED FROM SOMATOTROPE PF ANTERIOS LOBE PITUITARY
SITIMULATED BY SLEEP, STRESS , EXERCISE, HYPOGLYCEMIC, SOME OF FOODS

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GROWTH HORMONE

Sinthesized at somatotrope, pituitary acidophilic cells

191 aa, 22 kDa
5-15 mg/g of pituitary
GROWTH HORMONE AND PROLACTIN
GH EFFECT :

PROTEIN SYNTHESIS INCREASE

ANTAGONIZE INSULIN EFFECT

RELEASE FATTY ACID AND GLYCEROL FROM

ADIPOSE

RETENSION OF NATRIUM KALIUM AND CHLORIDE

STIMULATE LACTOGENESIS
PROLACTIN ACTIONS

LACTATION
LUTEOTROPIC HORMONE

OVERSECRETION OF PROLACTIN

AMENORHOE
GALACTORHOE
GYNECOMASTY
IMPOTENCE
CHORIONIC SOMATOMAMOTROPIN

PROLACTIN ACTIONS :
CS ACTIONS :
LACTATION
LACTOGENIC ACTIVITY
LUTEOTROPIC HORMONE

LUTEOTROPIC ACTIVITY

METABOLIC EFFECTS
OVERSECRETION SIMILAR :TO GH
OF PROLACTIN

INHIBITION GLUCOSE UPTAKE

AMENORHOE
GALACTORHOE
STIMULATION FATTY ACID RELEASE
GYNECOMASTY
NITROGEN AND CALCIUM RETENTION
IMPOTENCE
ANTERIOR PITUITARY HORMONE

ANTERIOR PITUITARY HORMONE CLASSIFICATION:

1. GROWTH HORMONE (GH), PROLACTIN (PRL) AND

CHORIONIC SOMATOMAMOTROPIN (CS)

2. GLYCOPROTEIN HORMONE
TSH, FSH, LH

3. PRO-OPIOMELANOCORTIN PEPTIDE FAMILY (POMC)

ACTH, LPH, MSH
GLYCOPROTEIN HORMONE

TSH
GONADOTROPIN (FSH, LH)
TSH, FSH, LH : CONSISTS OF TWO SUBUNIT : a AND b

Alfa subunit are same, beta subunit are different

WORKS THROUGH THEIR RECEPTOR AND ACTIVATION OF

ADEYLIL CYCLASE INCREASE OF cAMP
GONADOTROPIN (FSH, LH)

RESPONSIBLE FOR GAMETOGENESIS STEROIDOGENESIS

IN THE GONAD

FSH
TARGET : OVARIUM : FOLLICULAR CELLS
TESTES : SERTOLI CELLS

LH
TARGET : CORPUS LUTEUM, PRODUCE PROGRESTERON
LEYDIG CELLS, PRODUCE TESTOSTERON
THYROID HORMONE
HYPERTHYROID
THIROID HORMONE REGULATES :
GENE EXPRESSION

TISSUE DIFFERENTIATION

GENERAL DEVELOPMENT
THYROID HORMONE

T3 : 3,5,3’-TRIIODOTHYRONINE

T4 : 3,5,3’,5’-TETRAIODOTYRONINE (THYROXINE)

NEED TRACE ELEMENT : IODINE

THYROID CELLS
 METABOLISME YODIDA dalam FOLIKEL TIROID
RUANG FOLIKULER
DIT DIT
Oksid Perangk
asi Iodinasi MIT MIT T3 T4
I+ + Tgb
aian
Peroksidase DIT Tgb DIT DIT Tgb DIT
H2O2 MIT MIT MIT T4
DIT DIT
I-
O2 Pagositosis &
Tgb
NADPH NADP+ H+ Pinositosis

LISOSOM
Tgb

TIROSIN Lisosom
Tgb sekunder
I-
MIT Hidrolisa
I- DIT
POMPA YOD Kosentrasi * T3 & T4
Na-K ATPase Pelepasan
RUANG EKSTRASELULER T3 & T4
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I-
PRECURSOR OF T3 AND T4 : THYROGLOBULIN

PRODUCED BY FOLLICULAR CELLS OF THYROID GLAND

PRODUCTION STIMULATED BY TSH

PROTEIN 660 KDA, 5000 AMINO ACID

CONTAIN 115 TYROSINE RESIDUES FOR IODINATION

T4:T3 RATIO IN THYROBLOBULIN : 7:1

IOD DEFISIENSI : RATIO T4:T3 DECREASE
IODIDE METABOLISM

-CONCENTRATION OF IODIDE : IOD PUMP

-OXIDATION OF IODIDE : I- TO I+

-IODINATION OF TYROSINE : 3 AND 5 POSITION

-COUPLING OF IODOTYROSIS : DIT+DIT : T4

MIT+DIT : T3
THYROID HORMONE ARE TRANSPORTED BY THYROID-BINDING GLOBULIN

TBG : THYROXIN-BINDING GLOBULIN

GLICOPROTEIN, 50 KDA 100X AFFINITY OF TBPA, NONCOVALEN
BINDS T3 AND T4 100 TIMES AFFINITY TO TBPA
MORE IMPORTANT THAN TBPA

PRODUCE IN THE LIVER

STIMULATES BY ESTROGEN (PREGNANT AND PILS)
DECREASE DURING ANDROGEN OR GLUCOCORTICOID TX
ONLY SMALL AMOUNT OF FREE T3 AND T4

FREE T3 T4 : IMPORTANT FOR BIOLOGIC ACTIONS

RATIO T3:T4 IN BLOOD PLASMA: 1:1

80% T4 CONVERTED TO T3 IN CIRCULATION

(DEIODINATION)

T3 BINDS RECEPTOR 10 TIMES OF T4

T3 MORE IMPORTANT FOR BIOLOGIC ACTIVITY

THYROID HORMONE ACTION

ENHANCE PROTEIN SYNTHESIS

INDUCE GH TRANSCRIPTION

IMPORTANT FOR DEVELOPMENT

ELEVATED TSH :

CAUSED BY :

IODIDE DEFICIENCY
IODIDE EXESS
IODIDE TRANSPORT DEFECT
IODINATION DEFEXT
COUPLING DEFECT
DEIODINASI DEFICIENCY
PRODUCTION OF ABNORMAL IODINATION PROTEIN
GOITER
 ADRENAL HORMONE

MEDULA H. KATEKOLAMIN
ADRENAL
MINERALO-
GLAND 1. ZONA GLOMERULOSA
CORTICOID H.
CORTEX 2. ZONA FASICULATA
-HGLUCOCOR-
3. ZONA RETICULARIS TICOID H.
-ANDROGEN H.

CORTEX ADRENALIS

CORTICOSTEROID H. : 1. GLUCOCORTIKCOID
2. MINERALOCORTIKCOID
3. ANDROGEN ( SEX HORMON E) 55
 CORE OF STEROID  SIKLO PENTANO PERHIDRO PENENTREN
( 17 ATOM C )
12 17
11 13 16
C D
1 9 14 15 21 C C C C
2 10 8 20 C OHC C
OH
3 A 5 B 7 18
C
4 6
CH2 19
C=O
CHOLESTEROL
HO

HO

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PREGNENOLON
 BIOSINTESIS H. STEROID
KOLESTEROL

17-HIDROKSI DEHIDROEPIANDRO
PREGNENOLON
PREGNENOLON STERON ( DHEA )
3β-HIDROKSI STEROID DEHIDROGENASE : ∆5,4 ISOMERASE

POGESTERON 17-HIDROKSI PROGESTERON ∆4ANDROSTENE-

3,17-DION
21 - HIDROKSILASE

11-DEOKSIKORTI- TESTOSTERON
11-DEOKSIKORTISOL
KOSTERON ( DOC )

11-β-HIDROKSILASE
17-α-ESTRADIOL
KORTIKOSTERON KORTISOL

18-HIDROKSILASE-18-HIDROKSI
DEHIDROGENASE

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ALDOSTERON
HORMONES OF ADRENAL CORTEX

INTRACELLULAR RECEPTOR

REGULATE GENE EXPRESSION

ALTERRED PROTEIN SYNTHESIS

METABOLIC PROCESSES
GLUCONEOGENESIS
NATRIUM KALIUM BALANCE
GLUCOCORTICOID : CORTISOL
 SECRETION OF CORTISOL : DIURNAL RHYTHM BY ACTH STIMULATION

HIGH : AM, SHORTLY AFTER AWAKENING

LOWEST : LATE AFTERNOON,
EARLY EVENING

PLASMA TRANSPORT : TRANSCORTIN / CBG (CORTICOSTEROID BINDING

GLOBULIN)

EXCRETION : 70% URINE, 20% FECES, 10% SKIN

GLUCOCORTICOID ACTION :

1. INCREASE GLUCOSE PRODUCTION {GLUCONEOGENESIS)

2. INCREASE GLYCOGEN DEPOSITION
3. PROMOTE LYPOLYSIS
4. PROMOTE PROTEIN AND RNA METABOLISM

5. SUPPRESS IMMUNE RESPONS

6. SUPPRESS INFLAMATORY RESPONS

7. MAINTENANCE BLOOD PRESSURE AND CARDIAC OUTPUT

8. MAINTENANCE WATER AND ELECTROLITE BALANCE
9. RESPONS TO STRESS
GLUCOCORTICOID INSUFFICIENCY :

PRIMER : ADDISON’S DESEASE

HYPOGLYCEMIA, STRESS INTOLERANCE, ANOREXIA, WEIGHT LOSS,
NAUSEA , WEAKNESS, LOW BLOOD PRESSURE,
LOW GROMELURAL FILTRATION RATE, LOW PLASMA NATRIUM, HIGH
PLASMA KALIUM, LYPHOCYTE AND EOSINOPHIL INCREASE
HYPERPIGMENTATION (ACTH INCREASE POMC INCREASE)

SECONDARY : DECREASE ACTH (TUMOR INFARCTION OR INFECTION)

GLUCOCORTICOID EXCESS :

CUHSHING SYNDROME
HYPERGLYCEMIA, PROTEIN CATABOLISM, THINNING SKIN, MUSCLE
WASTING, OSTOPOROSIS, FULL MOON FACE, EDEMA , HYPERTENSION,
INFECTION
MINERALOCORTICOID : ALDOSTERONE
MINERALOCORTICOID : ALDOSTERONE

SECRETION : INDUCED BY ANGIOTENSIN, POTASIUM, ACTH , SODIUM

WEAK BINDING WITH ALBUMIN

EXCRESSION : CLEARANCE BY LIVER, EXCRETED IN THE URINE

ACTION

Na RETENTION, K, H, NH4 SECRETION

MINERALOCORTICOID EXCESS

PRIMERY :
CONN’S SYNDROME
HYPRTENSION, HYPOKALEMIA, HYPERNATREMIA, ALKALOSIS

SECONDARY
MINERALOCORTICOID EXCESS

PRIMERY :
CONN’S SYNDROME
HYPRTENSION, HYPOKALEMIA, HYPERNATREMIA, ALKALOSIS

SECONDARY
 ANDROGEN

ANDROGEN : DHEA (DEHYDROEPIANDROSTERONE),

ANDROSTENEDIONE, TESTOSTERONE
 HORMONES OF
ADRENAL MEDULA
CHROMAFFIN CELLS OF ADRENAL MEDULLA PRODUCE CATECHOLAMINES:

DOPAMINE, EPINEPHRINE, NOREPINEPHRINE

IMPORTANT FOR STRESS RESPONS

AFFECTED ORGANS: BRAIN, MUSCLE, CARDIOPULMONARY, LIVER

SKIN , GI TRACT, LYMPHOID
 CATECHOLAMINES
BIOSYNTHESIS

PNMT : phenylethanolamine
N-methyltransferase
LANGERHANS  α CELL : GLUCAGON HORMONE
 β CELL : INSULIN HORMONE

INSULIN HORMONE

INSULIN STRUCTURE IS PROTEIN, THAT IS CONSIST OF α –

POLIPEPTIDE AND β = POLIPEPTIDAE , HAVE TWO DIPEPTIDE BOND
and ONE DISULFIDE BOND IN THE α = PO LIPEPTIDE

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